The optimal management of neonates undergoing repair of complex congenital cardiac lesions requires detailed knowledge by the anesthesiologist of the anatomic and physiologic abnormalities and their consequences on the perioperative course. Management of these patients should not be undertaken in isolation but requires a concerted team approach for acceptable levels of mortality and morbidity to be obtained.

To determine whether the incidence of masseter muscle rigidity is affected by the anaesthetic induction sequence, we prospectively studied for ten months the anaesthetic course in 5,641 infants and children who received muscle relaxation to facilitate tracheal intubation. The anaesthetic induction sequence consisted of intravenous sodium thiopentone (STP) 5 mg.kg-1 alone, halothane induction alone 1-4%, or halothane followed by STP. Inhalational inductions with halothane included nitrous oxide and oxygen. Tracheal intubation was facilitated by either intravenous succinylcholine (Sch) at least 1.5 mg.kg-1 or by a non-depolarizing muscle relaxant. The induction sequence and all episodes of MMR were recorded. Ninety percent of the patients received Sch and 10% received a non-depolarising agent. Of those who received Sch, 88% (5,064 patients) were anaesthetised with STP and 12% (607 patients) were anaesthetised with halothane alone or halothane followed by STP. Masseter muscle rigidity was defined clinically by the transient inability to distract the mandible from the maxilla such that the mouth could not be opened or could only be opened with force. No children anaesthetised with STP followed by Sch developed MMR. One child (0.9%) developed MMR after halothane and Sch and two developed MMR after halothane, STP and Sch (0.4%). The incidence of MMR after Sch was less with STP than with halothane alone or with halothane and STP (P < 0.025). The peak CPK values in the three children who developed MMR were 17,580 IU.L-1 after halothane and Sch, and 7,280 IU.-1 and 3,273 IU.-1 after halothane, STP and Sch. There was no evidence of MH reactions in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

*Departments of Anaesthesia and Paediatrics (Cardiology), The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada, and the †Department of Anesthesia, The Children's Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A Address correspondence and reprint requests to Dr. Bruno Bissonnette, Department of Anaesthesia. The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, Canada M5G 1X8.

Percutaneous cannulation of the internal jugular vein in paediatric patients may be technically difficult and is prone to complications. To investigate the possibility that anatomical factors contribute to these difficulties, we used a two-dimensional ultrasound scanner to examine venous anatomy in children aged up to 6 yr. We found that 18% of our children had anomalous venous anatomy that may account for some of the difficulties reported previously. The diameter of the internal jugular vein was predicted poorly by the patient's age (r2 = 0.259) or weight (r2 = 0.155). We also evaluated the use of this ultrasound scanner during percutaneous central venous cannulation in neonates and infants. Determining the course of the internal jugular vein with the scanner and then marking it on the overlying skin reduced both the time and number of needle insertions required to aspirate jugular venous blood and increased the chance of a complication-free cannulation.

Profound hypothermic circulatory arrest and profound hypothermia with continuous low-flow cardiopulmonary bypass are used to facilitate repair of complex congenital heart lesions. Extended periods of profound hypothermic arrest may impair cerebral function and metabolism and produce ischemic brain injury. Low-flow bypass has been advocated as preferable to profound hypothermic arrest with respect to neurologic outcome as it maintains continuous cerebral circulation during repair of heart defects. Several studies have suggested that low-flow bypass produces equal degrees of cerebral injury as corresponding periods of circulatory arrest. Transcranial Doppler sonography has enabled the noninvasive study of cerebral perfusion during operations using either circulatory arrest or low-flow bypass. Although these studies have demonstrated the presence of cerebral perfusion at low perfusion pressures, evidence exists to suggest that cerebral perfusion abruptly ceases at cerebral perfusion pressures of 7 to 9 mm Hg and is unrelated to pump flow rate. Transcranial Doppler sonography is a useful tool for monitoring cerebral perfusion during low-flow bypass, and future studies with this modality may help to develop improved modes of cerebral protection during repair of complex congenital heart lesions.

Hillier, S. C. MB, FFARCS; Taylor, R. H. MB, FFARCS; Burrows, F. A. MD, FRCPC Author Information

Departments of Anaesthesia and the Research Institute, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada

Departments of Anaesthesia and the Research Institute, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada

Seven Yorkshire swine, ages 7–11 days and weighing 1.4–2.8 kg were studied to determine the effects of temperature and volume of injectate, depth of anaesthesia, position of the central venous catheter tip and vagotomy on the R-R interval after central venous injection of saline. The swine were anaesthetized with halothane in 100 per cent oxygen and their lungs ventilated to normocapnia. The length of the R-R varied inversely with the temperature of the injectate between 0 and 20° C reaching a maximum prolongation of 152 per cent above control values with 0° C saline. Injecting saline at 37° C did not affect the R-R interval. The length of the R-R interval varied directly with the volume of injectate between 1.5 and 4.5 ml· kg−1 (P < 0.05), The R-R interval response also varied directly with the depth of anaesthesia: the post-injection R-R interval increased from 185 per cent to 341 per cent as the end-tidal halothane concentration increased from 0.45 to 1.20 per cent. The position of the tip of the central venous catheter that produced the maximum increase in the R-R interval, as determined radiographically, was at the junction of the superior vena cava and the right atrium. Neither bilateral vagotomy nor atropine (50 μg · kg−1) affected the R-R interval after injecting 3 ml · kg−1 saline 0° C. We conclude that the increases in R-R interval after injection of fluid into the right atrium are due to direct effects on the nerve conduction system of the heart, possibly on the sinoatrial node.

To determine the effects of premedication on arterial oxygen saturation (SaO2) and heart rate (HR), 11 children (ages three to seven years) scheduled for elective repair of cyanotic congenital heart defects were studied. Patients were premedicated with oral or rectal pentobarbitone 2 mg.kg-1 90 minutes prior to induction of anaesthesia followed by intramuscular morphine 0.2 mg.kg-1 and atropine 0.02 mg.kg-1 60 minutes prior to induction. The SaO2 and HR of each child were monitored continuously using a Nellcor pulse oximeter during two 90 minute periods: a control period commencing 25.5 hours preoperatively (day 1) and a post premedication period commencing 1.5 hours preoperatively (day 2). Data were compared at time 0 (corresponding to the time of administration of pentobarbitone on day 2), 30 (corresponding to the administration of intramuscular morphine and atropine on day 2), 60 and 90 minutes (the latter corresponding to the time of induction on day 2) after the administration of pentobarbitone. There were no significant differences in SaO2 or HR between day 1 and day 2 at time 0, 60, and 90 minutes. The SaO2 (mean +/- SD) decreased significantly immediately following intramuscular premedication at time 30 minutes on day 2 (72.7 +/- 5.9 per cent) compared to the corresponding time on day 1 (83.9 +/- 2.9 per cent) (p less than 0.05). The duration of this desaturation was 2.5 +/- 1.9 minutes. Heart rate (mean +/- SD) increased from 109.2 +/- 21.3 beats.min-1 at time 30 minutes on day 1 to 142 +/- 20.4 beats.min-1 on day 2 (p less than 0.05). We conclude that administration of intramuscular premedication preceded by oral or rectal pentobarbitone causes transient arterial desaturation and tachycardia in children with cyanotic congenital heart disease.